A human SP-C promoter fragment targets α1-proteinase inhibitor gene expression to lung alveolar type II cells in transgenic mice

1996 ◽  
Vol 5 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Eric Degryse ◽  
Maria M. De Santi ◽  
Mireille Dietrich ◽  
Dalila Ali Hadji ◽  
Jean François Spetz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
Proteinase Inhibitor ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Promoter Fragment ◽  
Inhibitor Gene

scholarly journals Effects of bone marrow-derived mesenchymal stromal cells on gene expression in human alveolar type II cells exposed to TNF-α , IL-1β , and IFN-γ

2018 ◽  
Vol 6 (16) ◽  
pp. e13831 ◽  
Author(s):  
Matthew Schwede ◽  
Erin M. Wilfong ◽  
Rachel L. Zemans ◽  
Patty J. Lee ◽  
Claudia dos Santos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Tnf Α ◽  
Ifn Γ

scholarly journals Heparin Inhibits DNA Synthesis and Gene Expression in Alveolar Type II Cells

2002 ◽  
Vol 27 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Cheng-ming Li ◽  
Donna Newman ◽  
Jody Khosla ◽  
Philip L. Sannes
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

Influence of the cytoskeleton on surfactant protein gene expression in cultured rat alveolar type II cells

1998 ◽  
Vol 274 (1) ◽  
pp. L87-L96 ◽  
Author(s):  
John M. Shannon ◽  
Tianli Pan ◽  
Karen E. Edeen ◽  
Larry D. Nielsen
Keyword(s):  
Gene Expression ◽  
Protein Gene ◽  
Primary Cultures ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Partial Recovery ◽  
Type Ii ◽  
Alveolar Type Ii Cells

We have investigated the role of the cytoskeleton in surfactant protein gene expression. Cytochalasin D (CD), colchicine (Col), or nocodazole (Noco) were tested on primary cultures of adult rat alveolar type II cells. Treatment with any of the drugs did not result in dramatic cell shape changes, but ultrastructural examination revealed that the cytoplasm of cells treated with CD was markedly disorganized; cells treated with Col did not exhibit such changes. Treatment with any of the three drugs resulted in a reduction in surfactant protein (SP) mRNAs. These decreases were not the result of cell toxicity, since overall protein synthesis was unimpaired by drug treatment. Washing the cells followed by an additional 2 days of culture resulted in a reaccumulation of SP mRNAs in CD-treated cells but not in Col-treated cells. Washing of Noco-treated cultures resulted in partial recovery. SP mRNA stability was estimated in the presence or absence of cytoskeleton-disrupting drugs. Disruption of either microfilaments or microtubules significantly affected the half-lives of mRNAs for SP-A, SP-B, and SP-C. These data support a role for the cytoskeleton in the maintenance of type II cell differentiation and suggest that the role of the cytoskeleton is at least in part to stabilize SP mRNAs.

scholarly journals Gene expression of rat alveolar type II cells during hyperoxia exposure and early recovery

2007 ◽  
Vol 43 (4) ◽  
pp. 628-642 ◽  
Author(s):  
Zhongming Chen ◽  
Narendranath Reddy Chintagari ◽  
Yujie Guo ◽  
Manoj Bhaskaran ◽  
Jiwang Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Early Recovery ◽  
Alveolar Type Ii Cells ◽  
Hyperoxia Exposure

scholarly journals miR‐20a‐5p regulates pulmonary surfactant gene expression in alveolar type II cells

2019 ◽  
Vol 23 (11) ◽  
pp. 7664-7672 ◽  
Author(s):  
Yongjian Gong ◽  
Weidong Xu ◽  
Yang Chen ◽  
Yun Liu ◽  
Yuan Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Surfactant ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells

Impact of β-adrenergic agonist on Na+ channel and Na+-K+-ATPase expression in alveolar type II cells

1998 ◽  
Vol 275 (2) ◽  
pp. L414-L422 ◽  
Author(s):  
Yoshiaki Minakata ◽  
Satoshi Suzuki ◽  
Czeslawa Grygorczyk ◽  
André Dagenais ◽  
Yves Berthiaume
Keyword(s):  
Gene Expression ◽  
Atpase Activity ◽  
Continuous Treatment ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Short Term ◽  
Alveolar Type Ii Cells

It has been shown that short-term (hours) treatment with β-adrenergic agonists can stimulate lung liquid clearance via augmented Na+ transport across alveolar epithelial cells. This increase in Na+ transport with short-term β-agonist treatment has been explained by activation of the Na+ channel or Na+-K+-ATPase by cAMP. However, because the effect of sustained stimulation (days) with β-adrenergic agonists on the Na+ transport mechanism is unknown, we examined this question in cultured rat alveolar type II cells. Na+-K+-ATPase activity was increased in these cells by 10−4 M terbutaline in an exposure time-dependent manner over 7 days in culture. This increased activity was also associated with an elevation in transepithelial current that was inhibited by amiloride. The enzyme’s activity was also augmented by continuous treatment with dibutyryl-cAMP (DBcAMP) for 5 days. This increase in Na+-K+-ATPase activity by 10−4 M terbutaline was associated with an increased expression of α1-Na+-K+-ATPase mRNA and protein. β-Adrenergic agonist treatment also enhanced the expression of the α-subunit of the epithelial Na+ channel (ENaC). These increases in gene expression were inhibited by propranolol. Amiloride also suppressed this long-term effect of terbutaline and DBcAMP on Na+-K+-ATPase activity. In conclusion, β-adrenergic agonists enhance the gene expression of Na+-K+-ATPase, which results in an increased quantity and activity of the enzyme. This heightened expression is also associated with augmented ENaC expression. Although the cAMP system is involved, the inhibition of enhanced enzyme activity with amiloride suggests that increased Na+ entry at the apical surface plays a role in this process.

scholarly journals siRNA silencing of eotaxin‐3 (CCL26) modulates gene expression of eotaxin‐2 (CCL24) and CCR3 in alveolar type II cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
David M. Bauer ◽  
Equar Taka ◽  
Younes J. Effahali ◽  
Barack O. Abonyo ◽  
Ronald D. Thomas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Sirna Silencing

Gene Expression Profiles Of Alveolar Type II Cells From COPD Patients

2012 ◽  
Author(s):  
Naoya Fujino ◽  
Chiharu Ota ◽  
Takaya Suzuki ◽  
Satoshi Suzuki ◽  
Mitsuhiro Yamada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Copd Patients
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